Anti-tachycardia Pacing (ATP) has been used to convert ventricular tachycardias into normal sinus rhythm, but cannot always be relied upon to return the heart to normal sinus rhythm. Nonetheless, ATP is a standard treatment option to terminate most reentrant tachycardias. Also, ATP treatment has demonstrated high efficacy in terminating atrial flutter, however, it is very ineffective in terminating atrial fibrillation.
Atrial Fibrillation Arrhythmia
Atrial fibrillation (also referred to as “AF” or “afib”) is an abnormal heart rhythma—cardiac arrhythmia—of the two upper chambers of the heart. Heartbeats are normally initiated after electricity generated in the right atrium by the sinoatrial (SA) node spreads in an orderly manner over and through the heart to cause coordinated contraction of heart muscle and thus, pumping of blood. In atrial fibrillation, the regular electrical impulses of the sinoatrial node are replaced by disorganized, rapid electrical impulses that may result in irregular heartbeats.
Atrial fibrillation is one of the most common cardiac arrhythmias, but fortunately it is not as immediately serious as ventricular tachycardia. The risk of developing atrial fibrillation increases with age—atrial fibrillation affects four percent of individuals in their 80s. An individual may spontaneously alternate between atrial fibrillation and a normal rhythm (this is known as paroxysmal atrial fibrillation) or may continue with atrial fibrillation as the dominant cardiac rhythm without reversion to the normal rhythm (this is known as chronic atrial fibrillation). Atrial fibrillation is often asymptomatic, but may result in symptoms of palpitations, fainting, chest pain, or even heart failure. These symptoms are especially common when atrial fibrillation results in a heart rate that is either too fast or too slow. In addition, the erratic motion of the atria leads to blood stasis, especially in the atrial appendages, which predisposes to blood clots that may migrate from the heart to the brain and other organs. Thus, atrial fibrillation is an important risk factor for stroke, the most feared complication of atrial fibrillation.
Sometimes the symptoms of atrial fibrillation are treated with medications that slow the heart rate. Several medications as well as electrical cardioversion may be used to convert atrial fibrillation to a normal heart rhythm. Surgical and catheter-based therapies may also be used to prevent atrial fibrillation in certain individuals. Typically, patients with atrial fibrillation are given blood thinners such as warfarin to protect them from strokes.
Atrial fibrillation may be diagnosed on an electrocardiogram, in which characteristic findings (e.g., lead II of a rhythm strip) are: absence of P waves, unorganized electrical activity in place of the missing P waves, and irregularity of the R-R intervals due to irregular conduction of impulses to the ventricles. Holter monitoring (continuous ECG recording for 24 hours or longer) may be used to detect episodes of paroxysmal atrial fibrillation.
Pathophysiology of Atrial Fibrillation
The normal electrical conduction system of the heart allows an original impulse generated by the SA node to be propagated, stimulating the myocardium to contract as the impulse propagates from the SA node. The speed of the propagating electrical wave through various cardiac tissues and conduction bundles and the distance of the relative parts of the heart from the SA node or from a conductive bundle determine a sequential order according to which the different compartments of the heart are stimulated to contract. This ordered sequential contraction of the different parts of the heart causes efficient pumping. If the timing is off, then the pumping suffers or stops.
In atrial fibrillation, the regular impulses produced by the SA node to provide rhythmic contraction of the heart are overwhelmed by rapid randomly generated electrical discharges, e.g., as produced by larger areas of atrial tissue. Atrial fibrillation can be distinguished from atrial flutter, which is a more organized electrical circuit, usually in the right atrium, which produces characteristic saw toothed waves on an electrocardiogram.
In particular, atrial fibrillation can be caused and maintained by one or more “reentrant circuits” that produce the undesirable fibrillatory conduction. A reentrant circuit is typically a physical and electrical feedback loop composed of cardiac cells that repeatedly cycle electrical impulses in a tight circle and spin off abnormal impulses that propagate over the heart causing the disruption characteristic of atrial fibrillation. Such a problem feedback loop may be originated by a trigger, such as an abnormally occurring spontaneous depolarization of cell membrane in the myocardial tissue. Some reentrant circuits may come and go, may become chaotic for a few seconds, and then return, etc. However, most of these sources of atrial activation tend to be regular, and very consistent, or else atrial fibrillation would break of its own accord. A typical cycle duration for such a reentrant circuit is on the order of 100-200 milliseconds (ms). This is the equivalent of 600 beats per minute at a 100 ms cycle duration. If there is no such trigger and no resulting reentrant circuit, then fibrillatory conduction will not be there, i.e., the electrical conduction will be normal intrinsic conduction from an intrinsic rhythm (e.g., normal sinus rhythm).
Reentrant circuits can be further understood in terms of cellular action potentials continually propagating around the reentrant circuit at a rate considerably faster than the heart's intrinsic rate, provided that the reentrant wave front, i.e. the head of the propagation wave front, moves slowly enough that tissue ahead recovers excitability, i.e., slowly enough that a tail (or end of the propagation wave front) can form. The spatial extent of unexcitable tissue in this circuit is termed the reentrant wavelength, and is approximated by the product of the head's velocity and the action potential duration. As long as the wavelength is less than the circuit's perimeter, i.e. the reentrant path length, the head and tail remain separated by an excitable gap (of tissue waiting to be stimulated). Termination of anatomic reentry requires elimination of the excitable gap, which can be achieved by appropriate pacing. An appropriately timed stimulus (i.e., a pacing pulse) will initiate action potentials that propagate in both directions, colliding with the head and “blocking in” the tail.
In more simplified terms, the reentrant circuit can be thought of as a conduction wave front propagating along a tissue mass of somewhat circular geometry. This circular conduction will consist of a portion of refractory tissue and a portion of excitable tissue. To terminate the circuit, a pacing stimulus should be provided at the time and location when the tissue just comes out of refractoriness. If this occurs, the paced stimulation wave front proceeds toward the advancing wave front of the circuit, colliding with the wave front and interrupting the circuit. If the pacing stimulus (i.e., pacing pulse) arrives too soon it will be ineffective because the tissue will still be in refractoriness. If the stimulus arrives too late, it will generate wave fronts both towards the advancing wave front and towards the tail of the circuit. Although one pacing-generated wave front will collide with the advancing wave front of the reentrant circuit and will halt is progress, the latter pacing-generated wave front will act to sustain the reentrant circuit.
Conventional Treatments for Atrial Fibrillation
The main goals of treatment for atrial fibrillation are to prevent temporary circulatory instability and to prevent stroke. Rate and rhythm control are principally used to achieve the former, while anticoagulation may be required to decrease the risk of the latter. Rate control treatments aim to restore a normal heart rate, usually 60 to 100 beats per minute. Rhythm control seeks to restore the heart's normal rhythm, referred to as “normal sinus rhythm.” Rate control medications may include beta-blockers, calcium channel blockers and cardiac glycosides. These medications aim to slow down the impulses emanating from the atria and to slow down conduction of these impulses to the ventricles. Rhythm control techniques include electrical and chemical cardioversion. Electrical cardioversion applies a DC electrical shock to restore normal sinus rhythm. Chemical cardioversion relies on medications, such as amiodarone, propafenone, or flecainide, which make the heart tissue less excitable. These medications are sometimes used together with electrical cardioversion. Cardioversion poses the risk of systemic embolization by a blood clot from a location of previously stagnating blood, such as the previously fibrillating left atrium. Thus, cardioversion may require adequate anticoagulation in patients who have been in atrial fibrillation for more than a day or two.
When rate control medications are ineffective and normal sinus rhythm cannot be restored via cardioversion, then sometimes rate control is attempted by “ablation,” that is, destroying cardiac tissue responsible for the abnormal impulse production. In one alternative, this solution attempts to destroy the atrioventricular (AV) node—the group of cells electrically connecting the upper and lower chambers of the heart and serving as a re-transmitter of the SA node's original impulse. Electrical stimulation by an implanted cardiac device is substituted in its place.
In another variation of ablation, a technique tries to destroy groups of cells near the pulmonary arteries where atrial fibrillation is thought to originate. Or again, another technique tries to ablate relatively large areas of atrial tissue in an attempt to block atrial fibrillation from spontaneously arising. There are several other variations of the ablation technique. Radiofrequency ablation aims to destroy abnormal electrical pathways in the cardiac tissue—using RF energy. A radio-frequency emitting electrode is placed into the heart to destroy the tissue thought to be responsible for the abnormal electrical activity. Cryoablation freezes tissue to kill cardiac cells using a coolant that flows through a catheter. Microwave ablation does the same, but by heating the tissue to be destroyed. Such ablation techniques have gained popularity for atrial fibrillation that does not respond to the more conventional medication and cardioversion treatments.
The abnormal electrophysiology of atrial fibrillation can also be modified by surgically destroying cardiac tissue, and such procedures, such as the Cox maze procedure, are commonly performed concomitantly with cardiac surgery. More recently, minimally invasive surgical variations on the Cox Maze procedure (“minimaze” procedures) have also been developed.
The Cox maze procedure is an open-heart surgical procedure intended to eliminate atrial fibrillation, in which a series of incisions are made in the atria, the incisions made in a maze-like pattern. The intention is to eliminate atrial fibrillation by blocking potentially disruptive electrical circuits with non-conductive scar tissue. The Cox maze procedure is involved, using an extensive series of incisions inside of the heart, incisions through both atria, a vertical incision through the breastbone, and cardiopulmonary bypass (i.e., a heart-lung machine during the operation). Improved versions of the Cox maze procedure are now the state-of-the-art surgical treatment for atrial fibrillation
“Minimaze” techniques are miniature versions of the original maze procedure, and usually less invasive than the Cox maze procedure, not requiring a vertical incision in the breastbone or cardiopulmonary bypass. These procedures may use the aforementioned microwave, radiofrequency, or even acoustic energy to ablate atrial tissue near the pulmonary veins.
There are problems with these ablation techniques, even though many are favored as the state-of-the-art solution for atrial fibrillation. Clinicians typically ablate by performing a left side ablation, boring a hole through the atrial septum from right to left. The patient continues on anticoagulation therapy. The boring of a hole damages the heart itself, even though the damaged tissue may interrupt an abnormal conduction system and cure atrial fibrillation, at least temporarily. But such procedures can damage the heart (atrium) so much that it cannot contract effectively. Moreover, long-term efficacy of ablation has not been proven yet. The efficacy of AF ablation is thought to be around 60-85%, some even conjecture 90% efficacy. Atrial fibrillation can recur anytime, however. Thus, two undesirable consequences of ablation therapy include frequent reoccurrences and impairment of the mechanical action of the atria. Such may lead to stagnating blood in the atria—a silent recurrence that may give rise to stroke, the same feared complication of atrial fibrillation that the ablation technique sought to relieve.